Intestinal microvascular behavior during glucose absorption is characterized by dilation of villus arterioles to 120-125% of control after 1 1/2-2 minutes of glucose exposure and dilation of all other arterioles in the musculoris-submucosal tissues to 120-125% of control after 4-6 minutes. Tissue PO2 at the villus apex is decreased from a control of 13-16 mmHg to 6-9 mmHg whereas the control PO2 in the submucosal tissue of 26-29 mmHg is not appreciably altered. The responses listed are virtually identical for glucose concentrations 1/4 to 2 times the concentration reported for half-maximal glucose transport in vivo. The data are interpreted to indicate that tissue PO2 is not the sole cause of the 100% increase in blood flow during absorption. The temporal delay of dilation of the submucosal vessels after the start of glucose exposure is indicative of a mechanism that starts in the mucosa and gradually influences vessels in other areas of the intestinal wall. The proposed study will test the hypothesis that vasoactive agents such as absorbed sodium ion (coupled to glucose transport) and/or metabolically derived hydrogen ion diffuse from the mucosa to other layers of the intestine and cause dilation by a direct or osmotic effect. Ion selective microelectrodes will be used to measure the Na ion and H ion activity in the intestinal tissues during absorption as an index of mucosal to submucosal diffusion. The tissue activities of Na ion and H ion as well as tissue osmolarity will be artificially increased with suffusion solutions to the same activity as during absorption to estimate the vascular effect of these ions on the absorption hyperemia. The dilation of vessels at some distance from the mucosa may also be facilitated by cell-to-cell communication along arterioles. I propose that the mucosal environment causes dilation of mucosal vessels which communicate this dilation to up-stream vessels. This process has been seen to occur for distances of .5-2 mm following point source application of acetylcholine to single arterioles. These responses will also be compared to those in adult spontaneously hypertensive rats to detect alterations in vascular smooth muscle cell-to-cell communication as a result of the hypertensive process. These studies will be followed by an evaluation of intestinal absorptive hyperemia and skeletal muscle exercise hyperemia in innervated tissues of adult hypertens (Text Truncated - Exceeds Capacity)